we hypothesized that activating KRAS mutations and inactivation of the LKB1 oncosuppressor can cooperate to sustain NSCLC aggressiveness. We also hypothesized that the growth advantage of KRAS/LKB1 co-mutated tumors could be balanced by higher sensitivity to metabolic stress conditions, such as metformin treatment, thus revealing new strategies to target this aggressive NSCLC subtype.
|Titolo:||Metformin enhances cisplatin-induced apoptosis and prevents resistance to cisplatin in co-mutated KRAS/LKB1 Non-Small Cell Lung Cancer (NSCLC)|
|Data di pubblicazione:||2018|
|Appare nelle tipologie:||01.01 Articolo in Rivista|